BACKGROUND AND AIM: Gastrin is a growth factor for the gastric epithelial cells. However, it is unknown how gastric receptor (GR) expression is regulated in the gastric mucosa. We studied GR expression using a newly raised antibody and investigated the relationship between GR expression and gastritis. METHODS: Gastric receptor expression in 63 human gastric mucosa was studied. Helicobacter pylori infection and histological gastritis status were evaluated in gastric biopsy samples. In gastric ulcer cases, additional biopsy specimens were taken from injured mucosa. Fasting sera were collected and serum gastrin level evaluated. MKN-28 cells were cultured at various pH conditions, and the change in GR expression was determined. RESULTS: Gastric receptor expression was detected in the foveolar epithelium of the gastric mucosa, and its expression was stronger in patients infected with H. pylori. In particular, higher expression was detected in regenerating injured mucosa. There was no association between gastritis score/serum gastrin level and GR expression in H. pylori-positive cases. In MKN-28 cells, GR protein expression was lower in neutral conditions than in acidic or alkaline conditions. CONCLUSION: Gastric mucosal injury with H. pylori infection destroys the pH barrier on the foveolar epithelium and may induce GR expression through pH changes.
BACKGROUND AND AIM: Gastrin is a growth factor for the gastric epithelial cells. However, it is unknown how gastric receptor (GR) expression is regulated in the gastric mucosa. We studied GR expression using a newly raised antibody and investigated the relationship between GR expression and gastritis. METHODS: Gastric receptor expression in 63 human gastric mucosa was studied. Helicobacter pyloriinfection and histological gastritis status were evaluated in gastric biopsy samples. In gastric ulcer cases, additional biopsy specimens were taken from injured mucosa. Fasting sera were collected and serum gastrin level evaluated. MKN-28 cells were cultured at various pH conditions, and the change in GR expression was determined. RESULTS: Gastric receptor expression was detected in the foveolar epithelium of the gastric mucosa, and its expression was stronger in patients infected with H. pylori. In particular, higher expression was detected in regenerating injured mucosa. There was no association between gastritis score/serum gastrin level and GR expression in H. pylori-positive cases. In MKN-28 cells, GR protein expression was lower in neutral conditions than in acidic or alkaline conditions. CONCLUSION: Gastric mucosal injury with H. pyloriinfection destroys the pH barrier on the foveolar epithelium and may induce GR expression through pH changes.
Authors: H Kulaksiz; R Arnold; B Göke; E Maronde; M Meyer; F Fahrenholz; W G Forssmann; R Eissele Journal: Cell Tissue Res Date: 2000-02 Impact factor: 5.249
Authors: T C Wang; C A Dangler; D Chen; J R Goldenring; T Koh; R Raychowdhury; R J Coffey; S Ito; A Varro; G J Dockray; J G Fox Journal: Gastroenterology Date: 2000-01 Impact factor: 22.682